Evasion from apoptosis is critical for the development and expansion of malignant tumours. This was first shown for lymphomas that were elicited by deregulated expression of the cell cycle regulator c-MYC, which is abnormally over-expressed in ~70% of human cancers. Identifying the factors critical for the sustained growth of established MYC-driven lymphomas remains an important objective. In earlier work using Eµ-Myc mouse lymphomas and human Burkitt lymphoma (BL) we have demonstrated that tumour growth is dependent on the expression of the BCL-2 pro-survival family member, MCL-1 (Kelly et al G&D 2014). A new class of drugs termed BH3-mimetic drugs has been developed that can bind to BCL-2 pro-survival family proteins and induce death of cancer cells. We have assessed the efficacy and potential toxicities of a new BH3-mimetic drug targeting MCL-1. Our results suggest that targeting of MCL-1 could be an attractive therapeutic strategy for the treatment of MYC-driven lymphomas.